PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Cell Membrane Permeability”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 145 records · Page 8Linked to original sources
PubMed1984

Is renin secretion governed by the calcium permeability of the juxtaglomerular cell membrane?

Using cell cultures rich in renal juxtaglomerular cells we found that a change of the intracellular c-AMP concentration is not a prerequisite for an alteration of the renin secretion rate. Modulators of renin secretion including activators of the adenylate cyclase, however, altered the calcium permeability of the cellular plasma membrane in a way that stimulators of renin secretion lowered the calcium permeability and vice versa. Our results suggest that renin secretion is controlled by the intracellular calcium concentration and not by c-AMP. We postulate that modulators of renin secretion act by changing the calcium permeability of the cell membrane.

Angiotensin II↗
PubMed1993

[Control of membrane permeabilities in mammalian cells and its application to pharmaco-biology].

The plasma membrane in mammalian cells possesses unique permeability properties serving as a selective permeability barrier as well as transporters for nutrients and ions in maintaining cellular homeostasis. External ATP modulates the permeability barrier in transformed cells. The characteristics and possible mechanism for this permeability change are summarized. Application of this membrane change for cancer chemotherapy was also examined in both in vitro and in vivo. The uptake of D-glucose by mammalian cells was carried out by a facilitated diffusion through a specific transporter protein in the membrane. The control mechanism for glucose transport by growth factors based on the changes in the glucose transporter levels is summarized. Modulation of glycosylation in the transporter protein and its possible role are discussed.

Adenosine Triphosphate↗
PubMed2001

Cytolytic peptides induce biphasic permeability changes in mammalian cell membranes.

The cytolytic peptides melittin and gramicidin S are naturally occurring agents that provide a comparative model for studies of complement, immunotoxin and cell-mediated membrane permeability. Most attempts to characterize cytolytic peptides have used model membrane systems including phospholipid vesicles or erythrocytes. Membrane vesicles permit the use of self-quenching concentrations of fluorescent permeability markers, while erythrocytes release measurable hemoglobin. Attempts at measuring early membrane permeability changes in nucleated mammalian cells have been limited. To measure the kinetics of mammalian cell membrane permeability changes induced by cytolytic peptides, we developed a 96-well fluorescence cytolysis assay using the cytoplasmic fluorescent dye calcein as the membrane permeability marker. To facilitate rapid assessment of membrane permeability, trypan blue was added to the assay solution to quench (a) released fluorescence and (b) retained intracellular fluorescence. Trypan blue also provided a complementary visual assessment of cell viability. Using this assay, a detailed kinetic analysis demonstrated permeability of the cell membranes within seconds of exposure to the cytolytic peptides. The rapid permeabilization of the cell membranes was confirmed by flow cytometry using the calcium indicator dye fluo-3. The assay also demonstrated a second slower phase of marker release over the next several hours. The fluorescence cytolysis assay was able to reliably detect the biphasic permeability changes associated with the melittin and gramicidin S peptides suggesting the potential utility of this assay in the assessment of other cytolytic agents.

Animals↗
PubMedDate not supplied

Rhabdomyolysis associated with clozapine treatment in a patient with decreased calcium-dependent potassium permeability of cell membranes.

A 21-year-old patient developed rhabdomyolysis during his nineteenth week of treatment with clozapine for drug-resistant schizophrenia. No risk factors for rhabdomyolysis were found, but the calcium-dependent potassium efflux, normally responsible for membrane hyperpolarization and muscle refractoriness, was severely decreased in the patient's red blood cells. Clozapine is speculated to cause rhabdomyolysis in patients with defective calcium-activated K+ channels.

Adult↗
PubMed1973

Patterns of nonelectrolyte permeability in human red blood cell membrane.

The permeability of human red cell membrane to 90 different molecules has been measured. These solutes cover a wide spectrum of nonelectrolytes with varying chemical structure, chain length, lipid solubility, chemical reactive group, ability to form hydrogen bonds, and other properties. In general, the present study suggests that the permeability of red cell membrane to a large solute is determined by lipid solubility, its molecular size, and its hydrogen-bonding ability. The permeability coefficient increases with increasing lipid solubility and decreasing ability to form hydrogen bonds, whereas it decreases with increasing molecular size. In the case of small solutes, the predominant diffusion factor is steric hindrance augmented by lipid solubility. It is also found that replacement of a hydroxyl group by a carbonyl group or an ether linkage tends to increase permeability. On the other hand, replacement of a hydroxyl group by an amide group tends to decrease the permeability coefficient.

Amides↗
PubMed2006

Membrane electroporation theories: a review.

Electroporation, the transient increase in the permeability of cell membranes when exposed to a high electric field, is an established in vitro technique and is used to introduce DNA or other molecules into cells. When the trans-membrane voltage induced by an external electric field exceeds a certain threshold (normally 0.2-1 V), a rearrangement of the molecular structure of the membrane occurs, leading to pore formation in the membrane and a considerable increase in the cell membrane permeability to ions, molecules and even macromolecules. This phenomenon is, potentially, the basis for many in vivo applications such as electrochemotherapy and gene therapy, but still lacks a comprehensive theoretical basis. This article reviews the state of current electroporation theories and briefly considers current and potential applications in biology and medicine.

Animals↗
PubMed1994

Basolateral potassium membrane permeability of A6 cells and cell volume regulation.

The K+ permeabilities (86Rb(K) transport) of the basolateral membranes (JbK) of a renal cell line (A6) were compared under isosmotic and hypo-osmotic conditions (serosal side) to identify the various components involved in cell volume regulation. Changing the serosal solution to a hypo-osmotic one (165 mOsm) induced a fast transient increase in Cai (max < 1 min) and cell swelling (max at 3-5 min) followed by a regulatory volume decrease (5-30 min) and rise in the SCC (stabilization at 30 min). In isosmotic conditions (247 mOsm), the 86Rb(K) transport and the SCC were partially blocked by Ba2+, quinidine, TEA and glibenclamide, the latter being the least effective. Changing the osmolarity from isosmotic to hypo-osmotic resulted in an immediate (within the first 3-6 min) stimulation of the 86Rb(K) transport followed by a progressive decline to a stable value higher than that found in isosmotic conditions. A serosal Ca(2+)-free media or quinidine addition did not affect the initial osmotic stimulation of JbK but prevented its "secondary regulation", whereas TEA, glibenclamide and DIDS completely blocked the initial JbK increase. Under hypo-osmotic conditions, the initial JbK increase was enhanced by the presence of 1 mM of barium and delayed with higher concentrations (5 mM). In addition, cell volume regulation was fully blocked by quinidine, DIDS, NPPB and glibenclamide, while partly inhibited by TEA and calcium-free media. We propose that a TEA- and glibenclamide-sensitive but quinidine-insensitive increase in K+ permeability is involved in the very first phase of volume regulation of A6 cells submitted to hypo-osmotic media. In achieving cell volume regulation, it would play a complementary role to the quinidine-sensitive K+ permeability mediated by the observed calcium rise.

Animals↗
PubMed1999

Death signals from the B cell antigen receptor target mitochondria, activating necrotic and apoptotic death cascades in a murine B cell line, WEHI-231.

B cell antigen receptor (BCR)-mediated cell death has been proposed as a mechanism for purging the immune repertoire of anti-self specificities during B cell differentiation in bone marrow. Mitochondrial alterations and activation of caspases are required for certain aspects of apoptotic cell death, but how the mitochondria and caspases contribute to BCR-mediated cell death is not well understood. In the present study, we used the mouse WEHI-231 B cell line to demonstrate that mitochondrial alterations and activation of caspases are indeed participants in BCR-mediated cell death. The peptide inhibitor of caspases, N-benzyloxycarbonyl-Val-Ala-Asp-fluoromethylketone (z-VAD-fmk), blocked cleavage of poly(ADP-ribose) polymerase and various manifestation of nuclear apoptosis such as nuclear fragmentation, hypodiploidy and DNA fragmentation, indicating that signals from the BCR induced the activation of caspases. In addition, z-VAD-fmk delayed apoptosis-associated changes in cellular reduction-oxidation potentials as determined by hypergeneration of superoxide anion, as well as exposure of phosphatidylserine residues in the outer plasma membrane. By contrast, although z-VAD-fmk retarded cytolysis, it was incapable of preventing disruption of the plasma membrane even under the same condition in which it completely blocked nuclear apoptosis. Mitochondrial membrane potential loss was also not blocked by z-VAD-fmk. Bongkrekic acid, a specific inhibitor of mitochondrial permeability transition pores, suppressed not only the mitochondrial membrane potential but also the change of plasma membrane permeability. Overexpression of Bcl-xL prevented mitochondrial dysfunction, nuclear apoptosis and membrane permeability cell death triggered by BCR signal transduction. These observations indicate that death signals from BCR may first cause mitochondrial alterations followed by activation of both necrotic and apoptotic cascades.

Amino Acid Chloromethyl Ketones↗